INTESTINAL PEPTIDES AND THEIR MAIN ROLE IN THE PATHOGENESIS OF TYPE 2 DIABETES MELLITUS

Abstract

Diabetes mellitus, metabolic syndrome, obesity, hypertension, coronary heart disease are topical medical and social problems. Type 2 diabetes mellitus, especially complicated by diabetic angiopathy, is one of the leading causes of cardiovascular events, the development of end-stage chronic kidney disease with the need for hemodialysis, disability, and mortality. This review article summarizes information on the current understanding of the pathogenesis of type 2 diabetes mellitus. It has been shown that the achievement of stable compensation of carbohydrate metabolism without an increase in the frequency of hypoglycemic episodes, along with control of blood pressure and lipid spectrum, is a necessary condition for preventing the development and progression of type 2 diabetes mellitus. To date, it is known that the primary role in this belongs to the correct choice of the optimal hypoglycemic drug that can long-term support compensa- tion for type 2 diabetes mellitus and, if possible, favorably affect the main risk factors for damage to other body systems. From this position, it seems promising to study the role and place in the pathogenesis of type 2 diabetes mellitus of intestinal hormones - incretins, the main of which is glucagon-like peptide-1. In recent years, it has become known that glucagon-like peptide-1 not only regulates insulin and glucagon secretion in a glucose-dependent manner but is also directly able to stimulate natriuresis and the anti-inflammatory potential of the kidneys. In addition, the enzyme dipeptidypeptidase type 4, which is involved in the degradation of incretin glucagon-like peptide-1, metabolizes other hormone-like substances with vasoactive, immunomodulatory, natriuretic, and antioxidant properties. All this creates pathophysiological prerequisites for the search for potential protective properties in drugs that affect intestinal hormones.